中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (11): 1754-1755.doi: 10.4103/1673-5374.169608

• 观点:退行性病与再生 • 上一篇    下一篇

认知训练:对神经退性疾病的神经保护?

  

  • 收稿日期:2015-10-19 出版日期:2015-12-07 发布日期:2015-12-07

Cognitive training in neurodegenerative diseases: a way to boost neuroprotective molecules?

Francesco Angelucci*, Carlo Caltagirone, Alberto Costa   

  1. IRCCS Santa Lucia Foundation, Department of Clinical and Behavioural Neurology, Rome, Italy (Angelucci F, Caltagirone C, Costa A)
    Department of Systemic Medicine, Rome University Tor Vergata, Rome, Italy (Caltagirone C)
    Niccolò Cusano University, Rome, Italy (Costa A)
  • Received:2015-10-19 Online:2015-12-07 Published:2015-12-07
  • Contact: Francesco Angelucci, Ph.D.,f.angelucci@hsantalucia.it.

摘要:

神经退行性疾病的特点是一系列渐进的、明显不可逆的神经元损失或神经元功能丧失疾病。虽然每种神经退行性疾病都有不同的病理特征,对大脑的影响区域以及造成的结果也不尽相同,但其共同点是大脑神经元经历变性并逐渐死亡。现有的研究发现每种神经退行性变牵涉到许多基因或分子,如,已发现30多个基因与阿尔茨海默病显著相关,且这个数量还在快速增长。这些基因或分子可能是神经退行性变分子诱发神经损伤的调控或介导因子。对这些疾病的病因研究仍在进行之中,但遗憾的是并不容易找到可以遵循的正确方法。例如阿尔茨海默病,在没有达成任何明确结论的条件下,其数十年来的重点是“淀粉样蛋白级联假说”。当然直到今天,这一假设仍然有效,但有时也有必要转向其他研究方向。如,尸检研究已经清楚地表明淀粉样蛋白斑和神经纤维缠结症状是否也同样会发生在非阿尔茨海默病受试者身上?但对这些疾病机制的普遍看法来说,仍然像是缺了点什么。除了这些一般性考虑以及进一步研究的细节,提出和/或采用了的许多治疗方法中,一个共同的分母是尝试恢复,或至少限制神经元功能损伤。事实上,这是目前最合理的可循方法,正如我们之前提到的,这些疾病的原因还是一个未知数。
 

Abstract:

Neurodegenerative diseases comprehend a series of diseases characterized by progressive and apparently irreversible loss of neurons, or loss of neuronal functionality. Although each of these diseases has certain characteristics that affect different areas of the brain with different outcomes, the common denominator is that the brain neurons undergo degeneration and subsequent death. The study of the causes of these diseases is still ongoing, and unfortunately it is not easy to find the correct path to follow. As an example, it is worth to mention the case of Alzheimer’s disease (AD) where for decades the focus was on the “amyloid cascade hypothesis” without reaching any definitive conclusions. Naturally this hypothesis remains valid today but sometimes it is necessary to undertake other directions. How, for example, to explain the fact that post-mortem studies have clearly demonstrated the presence of amyloid plaques and neurofibrillary tangles in subjects without AD symptoms? It looks like something is missing to the general opinion on the mechanisms of these diseases. Besides these general considerations and going into further detail, among many therapeutic approaches proposed and/or adopted, a common denominator is the attempt to restore, or at least limit, the damage of neuronal function. Indeed, this is currently the most logical approach to follow, because as we said before, the causes of these diseases are still unknown. In this regard, we have recently proposed a cognitive rehabilitation protocol in patients with Parkinson's disease (PD), in which we used as a possible biomarker or readout of the effects of cognitive training the serum levels of a member of a class of proteins acting on neuronal function: the neurotrophin brain-derived neurotrophic factor (BDNF).